Acute effect of triiodothyronine on the dynamics of thyrotropin release from superfused anterior pituitary cells

The effects of triiodothyronine (T 3) on the dynamics of thyrotropin (TSH) release induced by TSH-releasing hormone (TRH) were examined in the presence or absence of a protein synthesis inhibitor, cycloheximide (CX), in a superfusion system using primarily cultured cells of the rat anterior pituitary gland on microcarrier beads. When the cells were continuously stimulated with TRH (10 nM, 180 min), TSH release occurred in a biphasic manner and the profile of TSH release was characterized by an initial sharp peak (phase I), followed by a lower plateau form phase (phase II). Both phase-I and phase-II releases were significantly suppressed in the presence of T 3 (1 ng/ml), which was added to the superfusion medium l h before initiation of TRH stimulation. The biphasic nature of the release profile was maintained in the presence of T 3, suggesting that the site of the T 3 action may be common between phase-I and phase-II release. We have already suggested that phase-I release is protein synthesis-independent and phase-II release protein synthesis-dependent using CX in TRH-stimulated cells. In the presence of CX, phase-I release was not suppressed by T 3, while phase-II release was still suppressed by T 3. The inability of CX to reverse the T 3-induced suppression of phase-II release may be masked by the direct CX effect on phase-II release of TSH. The present study indicates that each component (phase I and phase II) of the biphasic release of TSH induced by TRH stimulation was acutely suppressed by T 3 and suggests that the T 3 action is mediated through protein synthesis.